Miller D M, Cebulla C M, Rahill B M, Sedmak D D
Department of Pathology, The Ohio State University College of Medicine and Public Health, Columbus, OH 43210, USA.
Semin Immunol. 2001 Feb;13(1):11-8. doi: 10.1006/smim.2001.0291.
CD4(+)T lymphocytes are a significant component of the afferent and efferent arms of adaptive immunity and are critical for controlling viral infections. CD4(+)T lymphocytes secrete cytokines that augment CD8(+)T lymphocyte and B lymphocyte responses and directly inhibit viral replication. The interface between the CD4(+)T lymphocyte and virus is the major histocompatibility complex (MHC) class II molecule. Cytomegalovirus, a beta-herpesvirus, has evolved mechanisms for inhibiting MHC class II expression and thus escaping CD4(+)T lymphocyte immunosurveillance. Herein, we review cytomegalovirus-mediated down-regulation of inducible and constitutive MHC class II expression, while focusing on lesions that occur at the level of MHC class II transcription.
CD4(+)T淋巴细胞是适应性免疫传入和传出臂的重要组成部分，对控制病毒感染至关重要。CD4(+)T淋巴细胞分泌细胞因子，增强CD8(+)T淋巴细胞和B淋巴细胞反应，并直接抑制病毒复制。CD4(+)T淋巴细胞与病毒之间的界面是主要组织相容性复合体（MHC）II类分子。巨细胞病毒是一种β疱疹病毒，已进化出抑制MHC II类表达的机制，从而逃避CD4(+)T淋巴细胞免疫监视。在此，我们综述巨细胞病毒介导的诱导性和组成性MHC II类表达的下调，同时关注MHC II类转录水平发生的损伤。
